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Research Article Free access | 10.1172/JCI114528

Amylin secretion from the rat pancreas and its selective loss after streptozotocin treatment.

A Ogawa, V Harris, S K McCorkle, R H Unger, and K L Luskey

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.

Find articles by Ogawa, A. in: PubMed | Google Scholar

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.

Find articles by Harris, V. in: PubMed | Google Scholar

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.

Find articles by McCorkle, S. in: PubMed | Google Scholar

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.

Find articles by Unger, R. in: PubMed | Google Scholar

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.

Find articles by Luskey, K. in: PubMed | Google Scholar

Published March 1, 1990 - More info

Published in Volume 85, Issue 3 on March 1, 1990
J Clin Invest. 1990;85(3):973–976. https://doi.org/10.1172/JCI114528.
© 1990 The American Society for Clinical Investigation
Published March 1, 1990 - Version history
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Abstract

Amylin, a peptide copackaged with insulin in beta-cell granules, was measured in the effluent of the perfused rat pancreases by means of a newly developed specific radioimmunoassay. Its secretion parallels that of insulin in response to 20 mM glucose, 10 mM arginine, or the combination thereof. The relative molar amount of secreted amylin was estimated to be 25-37% that of insulin. Treatment with a borderline diabetogenic dose of streptozotocin reduced amylin response without significantly changing the insulin response. A severely diabetogenic dose of streptozotocin totally abolished amylin release and markedly reduced insulin release. The selective impairment of amylin secretion in streptozotocin-treated rats could represent an early manifestation of beta-cell depletion or injury.

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